Abstract
The oxidative burst is a critical early event in plant-pathogen interactions that leads to a localized, programmed cell death (PCD) called the hypersensitive response (HR). The HR and associated PCD retard infection by biotrophic pathogens, but can, in fact, enhance infection by necrotrophic pa- thogens like Botrytis cinerea. In addition to signaling the induction of the HR, reactive oxygen spe- cies (ROS) produced during the oxidative burst are antimicrobial. We hypothesize that pathogens such as B. cinerea survive the antimicrobial effects of ROS, at least partially by secreting the anti- oxidant mannitol during infection. This is supported by the previous observation that overexpres- sion of the catabolic enzyme mannitol dehydrogenase (MTD) can decrease a plants susceptibility to mannitol-secreting pathogens like B. cinerea. To extend the above hypothesis, and test the gen- eral utility of this approach in an important horticultural crop, we overexpressed celery MTD in tomato (Solanum lycopersicum cv. Moneymaker). In these studies, we observed a significant in- crease (up to 90%) in resistance to B. cinerea in transgenic tomatoes expressing high amounts of MTD.
Highlights
Botrytis cinerea is a necrotrophic fungus with a documented host range of more than 200 plant species [1] [2]
The hypersensitive response (HR) is initiated by the rapid, post-infection production of reactive oxygen species (ROS) and subsequent induction of programmed cell death (PCD) that limits the spread of infection [3] [4]
The amounts of mannitol dehydrogenase (MTD) expressed in plants transformed with a MTD-encoding transgene, were determined using protein blot analyses, and compared to levels found in wild type/untransformed (WT), and vector transformed (VT) plants
Summary
Botrytis cinerea is a necrotrophic fungus with a documented host range of more than 200 plant species [1] [2]. The HR is initiated by the rapid, post-infection production of reactive oxygen species (ROS) and subsequent induction of PCD that limits the spread of infection [3] [4] While it is an important defense against biotrophic pathogens, HR facilitates infection by necrotrophic pathogens like B. cinerea [5]. B. cinerea is itself reported to have an NADPH oxidase and a superoxide dismutase (SOD) [7] [8] that are activated, and presumably produce superoxide and hydrogen peroxide, respectively, as a part of the infection process We hypothesize that this additional ROS produced by B. cinerea can amplify the host plant HR/PCD and increase physical access for infection. This implies that B. cinerea has very effective protective mechanisms against ROS
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